ArticleAmerican journal of physiology. Renal physiology2010
Hypertension resistance polymorphisms in ROMK (Kir1.1) alter channel function by different mechanisms.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- A meta-analysis of gene expression signatures of blood pressure and hypertension.PLoS genetics · 2015Pooled it
- The endocytic adaptor ARH facilitates potassium conservation by regulating ROMK and BK.American journal of physiology. Renal physiology · 2025Article
- Pharmacologic ROMK Inhibition Protects Against Myocardial Ischemia Reperfusion Injury.International journal of molecular sciences · 2025Article
- Characterization of hyperactive mutations in the renal potassium channel ROMK uncovers unique effects on channel biogenesis and ion conductance.Molecular biology of the cell · 2024Article
- The role of uromodulin in cardiovascular disease: a review.Frontiers in cardiovascular medicine · 2024Review
- Genome mining yields putative disease-associated ROMK variants with distinct defects.PLoS genetics · 2023Article
- Phenotype of Idiopathic Infantile Hypercalcemia Associated with the Heterozygous Pathogenic Variant ofChildren (Basel, Switzerland) · 2023Article
- Kidney ion handling genes and their interaction in blood pressure control.Bioscience reports · 2022Review
- The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.Biomedicines · 2022Review
- Proanthocyanidins Maintain Cardiac Ionic Homeostasis in Aldosterone-Induced Hypertension and Heart Failure.International journal of molecular sciences · 2021Article
- Contributions of rare coding variants in hypotension syndrome genes to population blood pressure variation.Medicine · 2018Article
- Linking chanelopathies with endoplasmic reticulum associated degradation.Channels (Austin, Tex.) · 2017Article
- Emerging Targets of Diuretic Therapy.Clinical pharmacology and therapeutics · 2017Review
- Endoplasmic reticulum-associated degradation of the renal potassium channel, ROMK, leads to type II Bartter syndrome.The Journal of biological chemistry · 2017Article
- Role of renal transporters and novel regulatory interactions in the TAL that control blood pressure.Physiological genomics · 2017Review
- Isoforms of Spectrin and Ankyrin Reflect the Functional Topography of the Mouse Kidney.PloS one · 2016Article
- Lovastatin-Induced Phosphatidylinositol-4-Phosphate 5-Kinase Diffusion from Microvilli Stimulates ROMK Channels.Journal of the American Society of Nephrology : JASN · 2015Article
- Collecting duct principal cell transport processes and their regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- Rare mutations in renal sodium and potassium transporter genes exhibit impaired transport function.Current opinion in nephrology and hypertension · 2014Review
- Identification of compound heterozygous KCNJ1 mutations (encoding ROMK) in a kindred with Bartter's syndrome and a functional analysis of their pathogenicity.Physiological reports · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The renal outer medullary K(+) (ROMK) channel plays a critical role in renal sodium handling. Recent genome sequencing efforts in the Framingham Heart Study offspring cohort (Ji W, Foo JN, O'Roak BJ, Zhao H, Larson MG, Simon DB, Newton-Cheh C, State MW, Levy D, and Lifton RP. Nat Genet 40: 592-599, 2008) recently revealed an association between suspected loss-of-function polymorphisms in the ROMK channel and resistance to hypertension, suggesting that ROMK activity may also be a determinant of blood pressure control in the general population. Here we examine whether these sequence variants do, in fact, alter ROMK channel function and explore the mechanisms. As assessed by two-microelectrode voltage clamp in Xenopus oocytes, 3/5 of the variants (R193P, H251Y, and T313FS) displayed an almost complete attenuation of whole cell ROMK channel activity. Surface antibody binding measurements of external epitope-tagged channels and analysis of glycosylation-state maturation revealed that these variants prevent channel expression at the plasmalemma, likely as a consequence of retention in the endoplasmic reticulum. The other variants (P166S, R169H) had no obvious effects on the basal channel activity or surface expression but, instead, conferred a gain in regulated-inhibitory gating. As assessed in giant excised patch-clamp studies, apparent phosphotidylinositol 4,5-bisphosphate (PIP(2)) binding affinity of the variants was reduced, causing channels to be more susceptible to inhibition upon PIP(2) depletion. Unlike the protein product of the major ROMK allele, these two variants are sensitive to the inhibitory affects of a G protein-coupled receptor, which stimulates PIP(2) hydrolysis. In summary, we have found that hypertension resistance sequence variants inhibit ROMK channel function by different mechanisms, providing new insights into the role of the channel in the maintenance of blood pressure.
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